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Then, we investigated how many of these 53 genes were bound by AG using a publicly available AG ChIP-seq dataset40.
Over 90% of genes harboring H3K27me3 marks in WT cells had reduced H3K27me3 in Mtf2−/− CD71+Ter119-/lo pro-erythroblasts and nearly half (48.9%) of these genes were bound by Mtf2 at this stage of development (Fig. 3h).
In the contrary, we found that 7.6% of the Atf1/Pcr1-independent genes were bound by Atf1/Pcr1, which was less than 50% of the level by chance p-value<0.001 p-value<0.001
However, combined with the ChIP-on-Chip analysis, we found that only a fraction of those target genes were bound by SUZ12, one of the major components of the PRC2 complex.
We tested the promoter regions of the genes confirmed by qRT-PCR and found that seven of the ten upregulated genes were bound to their promoter region by Mecp2 (Fkbp5, Mobp, Plagl1, Ddc, Mllt2h, Eya2, and S100a9) (Fig. 3 and Figure S4).
Upon both treatments the cell-cycle arrest as well as the pro-apoptotic target genes were bound by p53 as shown in specific chromatin-immunoprecipitation experiments (Figure 1C), whereas chromatin-immunoprecipitations with IgG instead of a specific antibody did not result in a specific enrichment of target sites (Figure S1A).
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In view of the ubiquity of genetics in many research disciplines, with bioinformatics as its infrastructure, genes are bound to play a role in identity work.
It is possible that non-Ig genes are bound and deaminated by AID in Ramos.
The promoters of these genes are bound by Myc protein [13].
This was substantially higher than what would be expected considering that only 6% (141/2365) of all deregulated genes was bound by Ring1b.
And ∼34.2% of the Atf1-specific genes was bound by Atf1/Pcr1, which was more than 2-fold of the level by chance (p-value<0.01).
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